Objective. Children with iron poisoning, and mongrel dogs studied under laboratory conditions, were evaluated to explore the safety and effectiveness of the use of desferrioxamine in acute iron intoxication as reported in the 1965 paper.
Methodology. Twelve children admitted to a pediatric unit after iron ingestion were subjected to gastric lavage (10) and treatment either with intravenous desferrioxamine (9) or with a combination of intravenous and enteral (gavage) desferrioxamine (3). Serum iron levels before and after therapy, urinary excretion of iron, and symptoms before and after therapy were all measured.
Mongrel dogs (23) were fasted overnight and then given toxic doses of ferrous sulfate intraduodenally under general anesthesia. Controls (14) were observed for serum iron, arterial pH, and hematocrit, and mean arterial blood pressures. The 9 dogs treated were given desferrioxamine both intravenously and intraduodenally, whereas the controls were observed without treatment. Four additional dogs were treated with a lethal dose of iron that was first complexed with desferrioxamine and then administered intraduodenally. Another 2 dogs received a slow intravenous infusion of either ferrous or ferric iron, and 2 others were given the same amount of iron, but as a complex with desferrioxamine. Other studies were performed on dogs to evaluate the effect of desferrioxamine on arterial blood pressure and the toxicity of the iron-desferrioxamine complex.
Results. Rapid intravenous infusion produced hypotension in two children, one of whom had a seizure. Significant amounts of iron were discovered in the urine of all patients. None had progression of symptoms while in the hospital. One child who was in coma when admitted was noted to be developmentally retarded 5 months later.
All 14 control dogs died by 10 hours after duodenal instillation of iron. Three of the dogs treated survived, but these were the three with the lowest pretreatment iron levels. The enteral administration of lethal doses of iron previously complexed with desferrioxamine resulted in the excretion of large amounts of iron in the urine in 4 dogs and in one of three children treated with moderate amounts of iron complexed with desferrioxamine. The children were not affected adversely by this treatment, but the dogs experienced a marked drop in blood pressure and died within a few hours.
Conclusions. The use of desferrioxamine results in the rapid excretion of more iron in the urine than would occur without such treatment. The drug produces hypotension when administered rapidly by parenteral infusion. The enteral administration of the drug to poisoned dogs or children does not prevent the absorption of iron; indeed the complex is freely absorbable. The desferrioxamine–iron complex is toxic to the kidneys.COMMENTARY
Iron poisoning in lethal dose: Case report